Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.
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PMID:Hyperadrenocorticism in cats: seven cases (1978-1987). 284 Dec 69

A non insulin-dependent Zairian patient developed ketoacidosis and then overwhelming strongyloidiasis following ACTH treatment. Severe cardiovascular and respiratory failure, associated with severe acute hypoprotidemia, preceded death, which occurred within three days. Pathologic examination revealed a massive parasitic infiltration of the gastro-enteric mucosa, mesenteric lymph nodes, and the pulmonary tissue and vessels. We suggest that ACTH treatment and keto-acidosis induced immune deficiency and triggered the acute parasitic episode, in a patient originating from an endemic area. Badly controlled diabetes should be known as a risk factor of hyperinfection by Strongyloides stercoralis in latent carriers.
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PMID:Overwhelming strongyloidiasis in a diabetic patient following ACTH treatment and keto-acidosis. 284 5

Counterregulatory effect following administration of biosynthetic human proinsulin (BHPI) and human insulin (BHI) were compared during hypoglycemia standardized by means of a glucose controlled insulin infusion system (GCIIS). A total of 0.148 +/- 0.010 U/kg of BHPI had to be given by the GCIIS in order to obtain a minimal blood glucose (BG) of 26 +/- 2 mg/dl (means +/- SEM) at 43 +/- 2 min. In contrast, 0.083 +/- 0.004 U/kg of BHI were sufficient to produce a minimal BG of 21 +/- 1 mg/dl (n.s.) at 35 +/- 1 min. (P less than 0.005). Moreover, BHPI infusion resulted in prolonged hypoglycemia and delayed blood glucose recovery. On a molar basis, the acute BG lowering effect of BHPI was about 13% that of BHI (BHPI 3.94 +/- 0.27 vs. BHI 0.51 +/- 0.03 nmol/kg). Serum proinsulin after BHPI reached its maximum of 19.4 +/- 2 pmol/ml at 20 min. and still exceeded basal values markedly at the end of the test period at 240 min. Serum insulin peaked at 10 min. (162 +/- 47 microU/ml) and had already returned to basal values (7.5 +/- 1 microU/ml) after 45 min. No severe side effects were observed and there was no need for glucose administration, but clinical symptoms of hypoglycemia were more pronounced after BHPI. Compared to BHI, BHPI produced a higher cortisol peak (252 +/- 16 vs. 168 +/- 10 ng/ml), a more pronounced secretion of ACTH and GH as well as a stronger decline of serum potassium (3.20 +/- 0.06 vs. 3.58 +/- 0.08 mmol/l). Counterregulatory prolactin secretion did not differ significantly. Urinary epinephrine secretion following hypoglycemia after BHPI exceeded that after BHI (10.3 +/- 4.8 vs. 3.0 +/- 0.5 ng/120 min.). Serum lactate increase after BHPI was more prolonged (1.68 +/- 0.24 vs. 0.37 +/- 0.14 mmol/l at 120 min.). BHPI-induced inhibition of lipolysis, as determined by free fatty acid patterns, was delayed and less pronounced. Our results indicate that the observed more distinct glucose counterregulation is due to prolonged hypoglycemia rather than to any specific BHPI action on the hypothalamic-pituitary axis. We regard this as a consequence of the prolonged circulating and biological half-life. A preferential proinsulin action on the liver may play an additional role. Whether this "depot effect" may be beneficial in the treatment of diabetes mellitus remains to be established.
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PMID:Comparative study of hormonal counterregulation during GCIIS-guided hypoglycemia tests using human proinsulin and human insulin (recombinant DNA). 284 67

The effect on glucose homeostasis of a transient elevation of plasma growth hormone (GH) and cortisol was studied over 6 h in 14 male patients with insulin-dependent diabetes mellitus (IDDM) by using an i.v. somatostatin (100 micrograms/h) - insulin (0.4 mU/kg/min) glucose (3 mg/kg/min) - infusion test (SIGIT). GH (20 mU/kg) was given as a 60 min i.v. infusion during the initial SIGIT period raising the plasma GH level to about 40 micrograms/l, and returning to low basal within 3 h. ACTH (0.1 mg) was given as an i.v. bolus injection at the start of the SIGIT, resulting in plasma cortisol peak values of about 900 nmol/l within 2-3 h. GH raised blood glucose after a lag of 4 h while ACTH alone had no effect. However, ACTH added to GH enhanced the diabetogenic effect of GH. It is concluded that an episodic increase in circulating GH-cortisol, resembling the responses of these hormones to an insulin-induced hypoglycemia, exerts a diabetogenic effect in IDDM-patients not deprived of insulin. While GH is essential in this respect the diabetogenic effect of cortisol is evident only in conjunction with GH.
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PMID:Diabetogenic action of GH and cortisol in insulin-dependent diabetes mellitus. Aspects of the mechanisms behind the Somogyi phenomenon. 288 79

Because of its wide distribution in the organism, natural somatostatin (SRIF) demonstrates an ample spectrum of actions, involving mainly the central neuroendocrine system and the enteropancreatic area. In the former, this peptide may find its field of application in conditions characterized by excessive GH, TSH or ACTH secretion, depending on the central or peripheral cause of the inappropriate hormone control. The inhibitory effect of SRIF on gastrointestinal and pancreatic hormones may be useful in the management of tumors originating in this system and also in the treatment of inflammatory processes such as pancreatitis, in malignant diarrhea, and in gastrointestinal bleeding. A complex action of SRIF and its derivative on insulin release and glucose homeostasis may offer some advantages in the control of unstable diabetes. Dampening of organic functions in the upper digestive tract may also render SRIF and its analogues useful in the exploration of the gallbladder, gastric and pancreatic functions. The effect of such peptides on tissue growth and on the regulation of blood pressure are the subject of present investigations. Cytoprotection, an interesting aspect of SRIF application, is discussed elsewhere in this compendium. Finally, some comments on the possible use of SRIF as an additive to the conventional treatment of burns and sepsis close this review.
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PMID:Clinical applications of somatostatin. 290 Feb 4

The effects of a severe streptozotocin (STZ)-induced diabetes on the morphology and function of the adrenal zona fasciculata were examined in rats with intact or pharmacologically interrupted hypothalamic-hypophyseal-adrenal axis. In animals with an intact hypothalamic-hypophyseal axis, STZ-diabetes induced hypertrophy of the cells of the zona fasciculata and a rise in the plasma corticosterone concentration. Conversely, in rats in which the hypothalamic-hypophyseal axis had been interrupted, experimental diabetes provoked atrophy of the zona fasciculata cells, and a lowering in the plasma corticosterone level. The effects of STZ-diabetes were completely reversed by insulin infusion in both groups of rats. The hypothesis is discussed that the chronic lack of insulin may directly inhibit the growth and steroidogenic capacity of the rat zona fasciculata and that this effect of experimental diabetes may be masked in rats with an intact hypothalamic-hypophyseal axis by the concurrent enhancement of ACTH release due to chronic stress resulting from the metabolic consequences of prolonged diabetes.
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PMID:Effects of streptozotocin-induced experimental diabetes on the morphology and function of the zona fasciculata of rat adrenal cortex. 290 96

Lower concentrations of immunoreactive (IR) beta-endorphin were present in the neurointermediate pituitary lobes of streptozocin-induced diabetic versus control animals at both 2 and 4 weeks after the onset of diabetes. The forms of beta-endorphin-like material present appeared to be similar in both groups when studied with cation-exchange chromatography. Insulin therapy via minipump for 2 weeks did not alter this finding of lowered beta-endorphin concentrations in diabetic animals, despite normalization of blood glucose levels and body weight gain. Lower IR beta-endorphin levels were also found in neurointermediate lobes of weight-restricted rats, but this group had increased plasma IR beta-endorphin concentrations compared to diabetic animals. Concentrations of IR beta-endorphin in microdissected brain regions and in anterior pituitaries of the diabetic animals failed to show consistent changes; in addition, ACTH concentrations in pituitary lobes and plasma did not differ among groups. Circadian rhythmicity of plasma insulin and corticosterone concentrations was absent in the diabetic animals, although food and water intake, while elevated, showed the normal nocturnal pattern of increased ingestion. Furthermore, adrenal hypertrophy was present in the diabetic animals and was accompanied by an elevation of mean plasma corticosterone levels. The present findings indicate that diabetes is associated with a decrease of neurointermediate pituitary lobe synthesis of beta-endorphin, while not affecting the processing of the peptide in this lobe, and confirm previous reports of altered adrenal function in diabetic animals.
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PMID:Streptozotocin-induced diabetes is associated with reduced immunoreactive beta-endorphin concentrations in neurointermediate pituitary lobe and with disrupted circadian periodicity of plasma corticosterone levels. 299 96

Human insulin (BHI, recombinant DNA) and pork insulin (PI) were compared in 10 healthy volunteers. Using a glucose controlled insulin infusion system for the performance of the insulin hypoglycemia test (IHT), a comparable dosage of both insulins had to be infused (BHI 0.129 +/- 0.007 vs PI 0.115 +/- 0.01 U/kg; mean +/- SEM). Blood glucose slopes and nadirs did not differ significantly (BHI 30 +/- 2 vs PI 29 +/- 2 mg/dl). There was no difference in C-peptide inhibition (minimum for BHI 0.50 +/- 0.08 vs PI 0.42 +/- 0.08 micrograms/l). Maximum hormone responses were identical for ACTH (BHI 78.4 +/- 11.3 vs PI 76.0 +/- 8.7 pg/ml), cortisol (BHI 246 +/- 20 vs PI 252 +/- 15 ng/ml) and GH (BHI 43.8 +/- 7.3 vs PI 49.4 +/- 6.7 ng/ml). Peak levels of prolactin did not differ significantly (BHI 1,335 +/- 315 vs PI 1,766 +/- 614 microU/ml). The urinary excretion pattern of epinephrine in three 120 min periods before, during and after IHT was identical (before IHT: BHI 0.9 +/- 0.2 vs PI 0.6 +/- 0.1 micrograms/120 min; during IHT: BHI 12.6 +/- 2.2 vs PI 13.4 +/- 2.5 micrograms/120 min; after IHT: BHI 2.5 +/- 0.7 vs PI 3.7 +/- 1.3 micrograms/120 min). No differences in the minima of serum potassium levels were observed (BHI 3.38 +/- 0.04 vs PI 3.33 +/- 0.05 mmol/l). We conclude that the biological effects of human insulin and pork insulin are comparable. Our data do not support the assumption of a different hypothalamic handling of human insulin (recombinant DNA) and porcine insulin.
Diabetes Res 1985 May
PMID:Comparative study of hormonal counter-regulation during GCIIS-guided insulin hypoglycemia tests using human insulin (recombinant DNA) and pork insulin. 299 78

Renal handling of 125I-insulin was studied using a modification of the Sperber technique. Results showed 125I-insulin to be extracted at the peritubular side of the nephron in a process that was competitively inhibited by increasing amounts of unlabelled insulin, but not ACTH, in the injection mixture. When unlabelled insulin instead was injected 30 sec after the labelled insulin it showed significantly less interference with peritubular extraction of 125I-insulin, indicating strong attachment to the cell membrane or possible internalization of 125I-insulin into proximal tubular cells. Light microscope autoradiography 1 min after injection of 125I-insulin showed grains over proximal tubules only. On the ligated side localization was preferably peritubular while on the control side it was luminal. Electron microscope autoradiography showed sparsely distributed grains, however, frequently located over basal parts of proximal tubular cells. Pretreatment with lysine hydrochloride lowered renal extraction of 125I-insulin and increased urinary recovery of iodine label bilaterally. 125I-glucagon and 125I-C-peptide were not extracted from the peritubular circulation. In conclusion, the model has provided evidence of a rapid and significant peritubular extraction of 125I-insulin by proximal tubular cells in a process probably involving specific insulin receptors. Following receptor binding probably only minor amounts of 125I-insulin enters the proximal tubular cells, while the greater part is degraded at the cell surface or released into the circulation.
Diabetes Res 1985 May
PMID:Renal handling of 125I-labelled insulin in the hen. 299 79

Successive epinephrine infusions were used as a partial model to examine hormonal and metabolic responses to repeated stress stimuli. As both the endogenous opiates and epinephrine are released in response to stress, we have also studied interactions between epinephrine and B-endorphin. Epinephrine (0.1 microgram/kg . min) was infused for 60 min, followed by a 60-min recovery, in nine normal, conscious dogs. In a similar study, B-endorphin (0.06 microgram/kg . min) was given 30 min before epinephrine, then continuously infused throughout the study (N = 4 dogs). When epinephrine was infused, levels rose to 600-800 pg/ml. The changes in glucagon, B-endorphin, FFA, and hepatic glucose production were similar during both epinephrine infusions, but there was a diminished insulin response, a greater decrease in glucose metabolic clearance, and a greater increase in plasma glucose with the second epinephrine infusion. When B-endorphin was given, plasma levels increased to 5.3 ng/ml. Compared with the infusion of epinephrine alone, there was a much greater rise in plasma glucose due to greater suppression of glucose metabolic clearance. With the second epinephrine infusion, however, the changes in glucose concentration were not substantially different from those seen during the second infusion of epinephrine alone, as both hepatic glucose production and glucose metabolic clearance were suppressed. B-endorphin diminished the insulin and glucagon responses during the first epinephrine infusion and abolished them during the second, but did not alter the FFA, ACTH, or cortisol responses to epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Dec
PMID:Beta-endorphin modulation of the glucoregulatory effects of repeated epinephrine infusion in normal dogs. 299 13


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